We propose during the next year the following studies: 1) Our studies of the past year have shown a) that FSH induces testicular sensitivity to LH; b) that sensitivity to LH stimulation changes with sexual maturation. We hypothesize that FSH may act to induce sensitivity to LH by inducing formation of receptors to LH and propose to quantify LH-receptor populations during maturation and in our 5-day post-hypophysectomy immature rat model. 2) The immature male rat 5 days post hypophysectomy does not secrete biologically active androgens in response to LH stimulation. We propose to study the Leydig cell morphology to determine whether evidence of active secretion exists after 5 days of LH stimulation, and in the FSH pretreated animal. Other have postulated that non-biologically active steroids are secreted. These studies will indicate whether any Leydig cell response exists in the absence of exposure to FSH. 3) We propose to study whether the induction of sensitivity to LH is specific for FSH. Observation in various disease states in children suggests that factors other than chronological age correlate better with time of puberty (body weight, bone age, etc.). Thus, other hormones may play a role in this process too. We propose to study whether growth hormine, prolactin or ACTH may modify testicular response using our previously designed model. 4) We have shown that 5 days post hypophysectomy the immature female rat also becomes insensitive to LH. While FSH will (as in the male) restore sensitivity, it also will stimulate estrogen production. We propose to study the effects of very low doses of FSH (ineffective alone) on ovarian sensitivity to LH. 5) We propose to study the modulating effects of estradiol on pituitary secretion of LH in response to LRH. This will assist in interpreting whether the changes in LH and FSH observed during puberty are primary (causing gonadal response changes) or secondary caused by changing gonadal steroid concentrations).